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Biomedical subjects

C F Wooley

Publications and source records attributed to C F Wooley.

At least 73 records · Page 4Linked to original sources
PubMed1986

Evolution of a hereditary cardiac conduction and muscle disorder: a study involving a family with six generations affected.

This study describes six generations of a family with autosomal dominant cardiac conduction system and myocardial disease with recognizable clinical stages. A 20 year follow-up of nine family members, a medical questionnaire of 196, electrocardiographic screening of 91, noninvasive testing of 20, and catheterization with endomyocardial biopsy of six are the basis of this report. The clinical stages are as follows: Stage I occurs in the second and third decades of life and is characterized by an absence of symptoms, normal heart size, sinus bradycardia, and premature atrial contractions. Stage II is marked by first-degree atrioventricular block in the third and fourth decades. Stage III occurs in the fourth and fifth decades and is accompanied by chest pain, fatigue, lightheadedness, and advanced atrioventricular block followed by the development of atrial fibrillation or flutter. Stage IV, in the fifth and sixth decades of life, is characterized by congestive heart failure and recurrent ventricular arrhythmias. Light microscopy of right ventricular endomyocardial biopsy specimens from patients in stage II revealed very mild fibrosis; electron microscopy of the specimens demonstrated mild dilatation of tubules, mitochondrial swelling, and minimal myofibrillar loss. Biopsy specimens from patients with stage III disease were similar to those from patients with stage II disease except for an increase of myofibrillar loss. The stage IV specimens had diffuse fibrosis and more severe tubular dilatation, mitochondrial cristolysis, and myofibrillar loss. At autopsy in the proband, the atrial changes were more severe than the ventricular and were especially marked in the sinoatrial and atrial myocardium. Early recognition of the disease and use of pacemakers and antiarrhythmic agents have proved beneficial for affected family members. Thorough family studies of patients with conduction system disease and/or dilated cardiomyopathy are necessary to better understand the hereditary basis and natural course of this category of disease.

Adolescent↗
PubMed1985

Effect of acute standing and prolonged upright activity on left ventricular hemodynamics, systolic and diastolic intervals, and QT-QS2 relationship.

It is generally accepted that upright posture decreases preload and afterload, which could alter left ventricular (LV) performance. It is not known if changes occurring with acute standing persist after prolonged ambulatory activity (amb-act). In seven normal subjects echocardiographic end-diastolic and end-systolic diameters, percent shortening of the internal diameter (% delta D) and end-systolic wall stress (ES-WS), radionuclide diastolic volume and ejection fraction, preejection period over left ventricular ejection time (PEP/LVET), and diastolic time and QT-QS2 were measured supine, within 1 to 2 minutes after standing and after prolonged (60 minutes) amb-act. In addition, serial measurements were performed in PEP/LVET for 105 minutes at 15-minute intervals. With acute standing, end-diastolic diameter, diastolic volume, and ES-WS decreased (p less than 0.01); heart rate and PEP/LVET increased (p less than 0.01); while % delta D and ejection fraction remained unchanged. There was an inverse correlation between change in PEP/LVET and diastolic diameter (r = -0.59), but no correlation between PEP/LVET and ES-WS. The diastolic time per beat and per minute decreased (375 +/- 115 msec from 519 +/- 176 msec [p less than 0.01] and 31.3 +/- 4.2 sec/min from 33.7 +/- 4.5 sec/min [p less than 0.01]). The QT-QS2 increased when compared to supine (-7 +/- 7.6 msec from -22 +/- 7.7 msec [p less than 0.005]), but the QT-QS2 relationship remained normal (QT less than or equal to QS2). All the dynamic changes that occurred with acute standing tended to persist during prolonged amb-act.

Adult↗
PubMed1985

Tricuspid stenosis. Atrial systolic murmur, tricuspid opening snap, and right atrial pressure pulse.

Observations on the atrial systolic murmur, the tricuspid opening snap, and the right atrial pressure pulse of tricuspid stenosis are presented, based on catheter manometer intracardiac sound and pressure recordings in five patients with hemodynamically significant tricuspid stenosis. The manometer-recorded right atrial pressure pulse of tricuspid stenosis differed from the normal, with (1) elevation of right atrial pressure, (2) different morphologic features (tall, spiky A wave complete before C; small V wave with an interruption, the tricuspid opening snap notch at termination of the gradual Y descent; a diastolic plateau, the relatively flat diastolic segment of the right atrial pressure pulse following the tricuspid opening snap notch prior to the next A wave), and (3) the relative lack of right atrial pressure and right atrial pressure pulse response with normal respiration. The atrial systolic murmur, recorded in the right ventricular inflow tract, was complete by S1; the crescendo-decrescendo atrial systolic murmur configuration paralleled the right ventricular-right atrial diastolic pressure gradient at the time of the atrial A wave. The right atrial contraction-relaxation process, as reflected by the right atrial A wave ascent and descent, was complete at the onset of ventricular systole with P-R intervals of 170 to 200 msec. Thus, the timing and configuration of the atrial systolic murmur reflected the timing and completion of the right atrial contraction-relaxation process prior to the onset of right ventricular systole and the configuration of the tricuspid diastolic pressure gradient. The tricuspid opening snap was recorded in the right ventricular inflow tract and occurred at the time of a notch at the termination of the Y descent of the right atrial pressure pulse V wave, while right atrial pressure exceeded right ventricular pressure. The sound-pressure events were consistent with angiographic and echocardiographic studies, which showed doming or ballooning of the mobile, fused, stenotic tricuspid valve into the right ventricle during the Y descent of the right atrial pressure pulse. The tricuspid opening snap occurred at the time of the termination of the diastolic movement of the fused tricuspid unit into the right ventricle. These observations are presented within the framework of previous studies in order to trace the development of medical ideas about the pathophysiologic basis for the sound and pressure events of tricuspid stenosis.

Adolescent↗
PubMed1984

The electrophysiologic effects of upright posture.

In order to determine the effects of upright posture on the electrophysiologic properties of the human heart, 12 patients underwent electrophysiologic studies in the supine and upright positions. Compared to supine, the upright position significantly reduced basic cycle length from 818 +/- 111 to 680 +/- 141 msec, sinoatrial conduction time from 186 +/- 94 to 135 +/- 56 msec, corrected sinoatrial recovery time from 206 +/- 104 to 108 +/- 55 msec, interatrial conduction time from 76 +/- 17 to 70 +/- 16 msec, and the AV nodal conduction time (AH interval) from 88 +/- 19 to 78 +/- 14 msec (all p less than 0.05). Right intra-atrial and His-Purkinje (HV interval) conduction times were not altered. When the subjects assumed the upright position, the effective refractory periods of the right atrium, atrioventricular node, and right ventricle decreased significantly at basic and paced cycle lengths. For the group as a whole, the upright posture did not significantly augment repetitive responses to atrial and ventricular extrastimuli.

Adolescent↗
PubMed1984

Mitral valve prolapse: a marker for anxiety or overlapping phenomenon?

In symptomatic mitral valve prolapse patients (MVP): (1) the frequency and nature of symptoms were analyzed (n = 313); (2) metabolic studies were performed (n = 20), and (3) the response to isoproterenol infusions were studied (n = 16). Chest pain is more often the initial symptom in men; palpitations are more common initially in women. Fatigue, palpitations, dyspnea and arrhythmias are more frequent in women. Chest pain and neurologic events occur with the same frequency in both sexes. Women have more symptoms than men. MVP patients have normal thyroid function tests, normal plasma cortisol, normal diurnal variation of cortisol and normal 24-hour 17-ketosteroids and 17-hydroxycortico-steroids excretion. They have a normal response to oral glucose but higher glucose and insulin levels than controls. MVP patients have increased 24-hour urinary catecholamine excretion. Isoproterenol infusions produce symptoms in a dose-related fashion in MVP patients but not in controls. Isoproterenol infusion-related symptoms included chest pain (7), extreme fatigue (6), dyspnea (6), dizziness (4), numbness (2), panic attacks (2). Isoproterenol infusions produced a greater increase in heart rate in MVP patients compared to controls. Thus, MVP patients have increased catecholamines and hyperresponse to isoproterenol infusion which indicates that their symptoms may be catecholamine related or mediated. The complex relationships of MVP symptoms are not clear; the coexistence of anxiety states and MVP is one explanation; another equally plausible explanation is that MVP may be a specific marker for the symptom complex.

Adrenal Cortex Hormones↗
PubMed1984

Cardiovascular abnormalities associated with adult polycystic kidney disease.

In a combined retrospective and prospective study, 11 patients with adult polycystic kidney disease were found to have one or more cardiac or aortic lesions. Seven patients had primary dilatation of the aortic root and annulus with aortic regurgitation. The severity of the aortic regurgitation necessitated aortic valve replacement in 2. Mitral regurgitation was present in 3 patients, of whom 2 had documented redundant mitral leaflets and ruptured chordae tendinae, and the third had mitral valve prolapse. Histologic analysis of available aortic and mitral valve tissue from these acquired lesions showed myxomatous degeneration with loss and disruption of collagen. Four patients had congenital bicuspid aortic valves with aortic regurgitation; 1 of these patients also had mild valvular stenosis, and 1 had coarctation of the aorta.

Adult↗
PubMed1983

Mitral valve prolapse syndrome: analysis of 62 patients aged 60 years and older.

Sixty-two patients diagnosed as having mitral valve prolapse, 60 to 81 years old, presented with disabling chest pain (20), symptoms of arrhythmias including palpitations and syncope (16), or mitral regurgitation (MR) with symptoms of congestive heart failure (26). The diagnosis of MVP was made on the basis of a combination of classic auscultatory, echocardiographic and angiographic findings. Thirteen of the 20 patients with chest pain had normal coronary angiograms and 7 had significant coronary artery disease (CAD). Patients with CAD could not be differentiated by clinical presentation alone. Furthermore, the incidence and types of arrhythmias, the presence of a positive stress test, and hemodynamic findings were similar in all patients in this group whether or not CAD was present. The 16 patients with palpitations had a broad spectrum of rhythm disorders, including both supraventricular and ventricular arrhythmias. Two patients had prehospital "sudden death" and 2 others had systemic emboli. Twenty-one of the 26 patients with MR had valve surgery. Intraoperatively the valves were described as enlarged, floppy and with redundant leaflets. Histologic examination showed extensive "myxomatous" changes throughout the valve leaflets. Thus, mitral valve prolapse is a cause of symptomatic heart disease in the elderly. It has a predictable pattern of clinical presentation and should be considered in the differential diagnosis of older patients with disabling chest pain and arrhythmias and as the cause of progressive or severe MR.

Aged↗
PubMed1983

Acute massive (pericardial effusive) pulmonary thromboembolism--pulmonary embolectomy revisited.

The most recent patient in a 13-year experience with 14 patients suffering massive pulmonary thromboembolism requiring pulmonary thromboembolectomy is the focus of this report. This 40-year-old woman not only survived life-threatening acute hypoxemia and right heart failure, but was also found to have developed a unique transudative 700 cc pericardial effusion. Pulmonary artery pressure was 90/30 (mean 50 mmHg), accompanied by 17 mm right ventricular alternans. Systemic alternans and tamponade physiology were absent. This unusual natural model for acute right heart failure illustrates a novel mechanism for pericardial effusion physiology.

Adult↗
PubMed1983

The mitral valve prolapse syndrome.

In clinical perception, the syndrome has evolved from a neuropsychiatric disorder to a medical disease with an anatomic basis. Still unanswered is whether the autonomic and adrenergic dysfunctions that occur in some patients are an intrinsic part of the syndrome or of an unrelated anxiety neurosis. Pending clarification, both medical and psychological aspects require attention.

Adolescent↗
PubMed1982

Jacob Mendez DaCosta: medical teacher, clinician, and clinical investigator.

J. M. DaCosta, a scholarly, well-trained and observant clinician, was recognized during his lifetime as a well-known authority on physical diagnosis and had an unexcelled reputation as a clinical teacher. Chairman of Medicine at the Jefferson Medical College for 19 years, president of the College of Physicians of Philadelphia in 1884 and again in 1895, he was one of the original members of the Association of American Physicians and its president in 1897. Earlier in his career, his extensive Civil War study of "a form of cardiac malady common among soldiers . . . the study of which is equally interesting to the civil practitioner" was described in his 1871 paper "On Irritable Heart; A Clinical Study of a Form of Functional Cardiac Disorder and Its Consequences." Soon labeled DaCosta's syndrome, the irritable heart lineage can be traced through the soldier's heart, the effort syndrome, and neurocirculatory asthenia in World War I, anxiety neurosis in World War II, and the mitral valve prolapse syndrome in the second half of the 20th century.

Cardiology↗